Personal Historical Perspective
2003 to 2012 – In 2003 prior to undertaking Physiotherapy at the University of Queensland, I completed an assignment with three other students as an assessment item for Advanced Topics in Functional Anatomy, a course convened by Vaughan Kippers, who was the primary anatomy lecturer for physiotherapy students. I was undertaking this course as a pre-requisite before undertaking the Graduate Entry Masters Physiotherapy program at University of Queensland. The assignment was titled:
“The Segmental Lumbar Stabilisation System as it Relates to Treatment of Low Back Pain”
My two contributions were the introduction and:
“The Local Lumbar Segmental Stabilization System: From Historical Development to Methodological Considerations for Future Research”
The assignment was marked by Vaughan Kippers himself who awarded my contribution full marks, while overall the group received the highest mark in the class. To demonstrate my long-term interest in exercises for the treatment and prevention of low back pain (LBP), I have included my contribution to the assignment in appendix one.
LBP: A Paradigm Shift
2013 – to present. My approach to exercises for low back pain (LBP) for several years after graduating as a physiotherapist was based on University of Queensland’s segmental lumbar stabilization approach (for a summary of this approach see my 2012 post here). However, I have since undergone a paradigm shift in my thinking on back pain – its cause and its treatment. I was exposed to the idea that paraspinal/erector spinae muscle tension might be a rather more important cause of back pain than the inhibition of muscles proposed to be lumbar stabilizers. The genesis of this came from experience with two Chinese internal martial/healing arts teachers, both from several centuries’ old lineages, who suggested that unnecessary trunk muscle tension, especially in the back muscles, was by far the most important foundational cause of back pain. My approach to the treatment of back pain now is primarily to decrease unnecessary back muscle tension, to improve circulation in the lower back region, and to teach therapeutic and functional exercises that support these goals. These techniques are drawn from Chinese internal martial/healing arts, such as Qigong and Tai Chi, as well as Western techniques such as reciprocal inhibition.
Bipedalism Per Se May Cause Erector Spinae Tension Leading to Pathology
Formative in the development of my afore mentioned approach is the finding that in non-human primates, Japanese Macaques, the erector spinae are “far more strongly activated [and] coactivated during the entire step cycle…” in bipedal compared to quadrupedal gait because these muscles are needed to “…control body axis pitch [and] counteract mediolateral body sway against gravity” (Higurashi et al., 2019). This suggests that the adoption of bipedal locomotion per se requires a high level of back muscle recruitment.
This idea is supported by the spinal neurosurgeon and evolutionary biologist, Aaron Filler, who noted from the fossil evidence that in obligate bipeds such as humans and other now extinct hominins, the evolutionary drive towards efficiency of bipedal movement resulted in substantial increases in the size and strength of the iliocostalis and longissimus, the muscles that comprise the erector spinae, which allowed hominins to be “…better able to position and balance the upper body over the pelvis during walking, running, and carrying” (Filler, 2007). These evolutionary changes, as necessary as they were, nevertheless came “…at the cost of greatly increased compressive stress on the vertebral disks” (Filler, 2007).
The Myth of Lumbar Instability as a Cause of Low Back Pain: Mullholland’s Observation
Making a similar observation to Filler (2007), without the evolutionary perspective, another spinal surgeon, Robert Mulholland, wrote “As the loads on the back are mostly produced by muscle action rather than body weight, activities that involve strong muscle action, such as lifting, are associated with pain” (Mullholland, 2008). In support of this statement, Mullholland (2008) cited studies that “…showed very clearly the close relationship of posture and stress in the disc, and …demonstrated the important effects of muscle action on these stresses” (Nachemson et al., 1975; Schulz et al.,1982).
Mullholland’s article, titled “The myth of lumbar instability: the importance of abnormal loading as a cause of low back pain”, was a critique of the idea that spinal instability is a common cause of back pain and an assertion that the published evidence suggests that loading of the spine by muscle action was, in contrast, a common cause (Mullholland, 2008). Mullholland’s critique extended to the published work of the influential biomechanist, Manohar Panjabi, whose theories were foundational in the development of the segmental lumbar stabilization exercise approach to the treatment of back pain developed by University of Queensland that I reviewed in my 2003 assignment (see appendix one) (Mullholland, 2008; Panjabi et al., 1989; Panjabi, 1992; Richardson & Jull, 1995; Richardson et al., 1999; Richardson, Hodges, & Hides, 2004).
The Myth of Lumbar Multifidus Atrophy as a Cause of Low Back Pain: Dreyfus et al.’s Observation
Another factor in my move away from spinal stabilizing exercises for LBP was the evidence that contradicts the assumption that the atrophy of the lumbar multifidus causes LBP (Dreyfus et al., 2009). The inhibition and atrophy of the lumbar multifidus in LBP was first observed by Hides et al, (1994). Hides, Richardson, & Jull (1996) observed that the same was true of first-episode LBP sufferers. Based on in vitro cadaver modelling evidence it was determined that the lumbar multifidus acted as lumbar stabilizer (Wilke et al., 1995). Based on biomechanical theory it was assumed lumbar multifidus inhibition would lead to lumbar instability related LBP (Panjabi et al., 1989; Panjabi, 1992; Richardson & Jull, 1995; Richardson et al., 1999; Richardson, Hodges, & Hides, 2004).
The evidence to the contrary comes from Dreyfus et al. (2009) who, using radiofrequency neurotomy deliberately denervated the medial branch of the dorsal ramus in LBP sufferers. This procedure is routinely performed to relieve facet joint derived LBP (Russo, 2021). However, since this is the nerve that supplies the multifidus, it also causes denervation inhibition of these muscles (Dreyfus et al., 2000). Six weeks after the neurotomy, which blinded radiographers confirmed caused inhibition of the multifidi innervated by the targeted nerves, visual analogue scores found 80% relief from the pain the patients sought the surgery for. This relief was maintained one year post neurotomy. These data:
…indicate that lumbar medial branch neurotomy is a safe procedure and refute concerns raised in the literature that medial branch neurotomy could cause instability and pain. More generally, however, the results of the present study challenge the significance of multifidus atrophy as implied in the literature. (Dreyfus et al., 2009)
To the authors knowledge the published evidence to date has not found a causal link between multifidus atrophy and pain (Dreyfus et al., 2009; Sadeghi, Bible, & Cortes, 2020). Such a link might exist and might be established in the future, however, considering the painful consequences of the types of pathology proposed to cause multifidus atrophy, e.g., dorsal ramus impingement (Annaswamy, Bierner, & Doppalapudi, 2013; Kader, Wardlaw, & Smith, 2000) or intervertebral disc pathology (Hodges et al., 2006), it seems reasonable to propose that multifidus atrophy is a consequence, rather than a cause, of painful pathological processes. Processes that may have their genesis in paraspinal/erector spinae tension.
Furthermore, regarding potential causes of dorsal ramus impingement, it is worth considering that “dorsal ramus syndrome”, defined as LBP pain arising from impingement of the dorsal ramus, while usually associated with facet joint pathology, can have other causes including “lumbar paraspinal muscle spasms” (Annaswamy, Bierner, & Doppalapudi, 2013). Such spasms can also be regarded as a primary cause of lumbar disc damage (vide supra) (Filler, 2007; Mullholland, 2008). Hence the primary cause of dorsal ramus syndrome pain, discogenic pain, and multifidus inhibition/atrophy may be paraspinal/erector spinae tension.
Cluneal Nerve Derived Pain Caused by Paraspinal/Erector Spinae Tension
It is worth noting that while the medial branches of the dorsal ramus supply the facet joints, the lateral and intermediate branches, pierce the erector spinae and are thus subject to entrapment from sustained contraction, pressure, or spasm of this muscle (Wu et al., 2023; Iwanaga et al., 2018; Zhou, Shneck, & Shao, 2012; Lauschke & Major; 2016). The lateral branches of the dorsal ramus continue through the iliocostalis, or the junction between the iliocostalis and the longissimus, and pierce the thoracolumbar fascia just cephalad or caudad to the posterior iliac crest, where upon their designation becomes the superior cluneal nerves (Karl et al., 2022). In contrast, the middle cluneal nerves “traverse” the erectors spinae, leave the spine through the sacral foramen, and pierce the long sacroiliac ligament (Tubbs et al., 2010; Konno et al., 2017). The superior and middle cluneal nerves provide sensation to the lower back in the region of the sacroiliac joint, posterior superior iliac spine, and buttocks.
Entrapment of the superior cluneal- and middle cluneal-nerves can occur in the thoracolumbar fascia and long sacroiliac ligament, respectively (Isu et al., 2018). Because the origins of these nerves can also be entrapped in the erector spinae spinae, this creates the conditions for a double/multiple crush syndrome whereby compression of axons at one location increase their vulnerability to compression at another (Tubbs et al., 2010: Wu et al., 2023; Molinari & Elfar, 2013). It seems reasonable to propose that compression of superior and middle cluneal nerves towards their origin in the paraspinal/erector spinae type is the dorsal ramus impingement from “lumbar paraspinal muscle spasms” referred to by Annaswamy, Bierner, & Doppalapudi (2013).
Compression of the cluneal nerves either in the erector spinae or more distally can cause pain in lower back and posterior buttocks, extend laterally to the trochanteric region, anteriorly to the anterior hip region, and distally to the lower limbs as far as the feet (Iwanaga et al., 2018; Isu et al., 2018; Karl, Helm, & Trescot, 2022; Maigne & Nieves, 2006). Compression of the superior and middle cluneal nerves can be difficult to distinguish between nerve root pain from a herniated disc (Aota, 2016; Matsumoto et al., 2021; Konno et al., 2017). This suggests LBP diagnosed as being caused by disc herniation may instead be caused by superior and/or middle cluneal nerve compression (Aota, 2016; Matsumoto et al., 2021; Konno et al., 2017). In response to these findings Konno et al. (2017) and Fujihara et al. (2021) used the term “Pseudosciatica” to describe superior and middle cluneal derived pain that mimicked disc herniation derived sciatic pain.
As noted above, the cluneal nerves can be entrapped by the thoracolumbar fascia. Indeed, most of the literature documenting the surgical treatment of cluneal nerve entrapment is from compression at this site (Wu et al., 2023; Isu et al., 2018). It is also worthwhile noting that the actions of the erector spinae tensions the thorocolumbar fascia increasing the likelihood of this fascia compressing the cluneal nerves (Speed, Sims, & Weinrauch, 2011). This mechanism was outlined by two Brisbane based orthopaedic surgeons and a physiotherapist who published a case study of a cricket fast bowler with cluneal nerve compression that when surgically released yielded a full recovery from pain and return to full function (Speed, Sims, & Weinrauch, 2011). Highlighting the importance these authors assigned to erector spinae tension as the cause of cluneal compression related LBP is their statement: “We believe that the superior cluneal nerve may be susceptible to compression related repetitive contraction of the back musculature, in particular the Thoraco-lumbar erector spinae” (Speed, Sims, & Weinrauch, 2011).
Conclusions and Directions for Future Research
Taken together, these data suggest that paraspinal/erector spinae tension giving rise to disc-, dorsal ramus-, or cluneal-nerve compression may be an underappreciated and quite common primary cause of LBP. Furthermore, while these data do not exclude the possibility that exercises designed to engage supposed lumbar stabilizers or other trunk muscles are a useful addition to therapeutic exercise for LBP, they do suggest that exercises designed to decrease paraspinal/erector spinae tension and promote circulation in these compartments warrant further research investigation.
These data also suggest that repeated execution of exercises designed to improve lifting technique, such as deadlifts, for the purpose of preventing LBP may inadvertently create it by increasing resting intramuscular pressure in the erector spinae compartment and/or increasing tension in the thoracolumbar fascia thus causing nerve or disc compression related pathology (Ramirez et al., 2022; Roe, Chen, & Cho, 2018; Speed, Sims, & Weinrauch, 2011).
I would like to conduct/supervise research on the effects of therapeutic exercises designed to decrease the tension and improve circulation in the paraspinal/erector spinae muscles. This is an important line of research, given the gaining popularity of the “deadlift” and similar exercises designed to strengthen the back muscles (Steele, Bruce-Low, & Smith, 2015; Aasa et al., 2015; Fischer, Calley, & Hollman, 2021; Ramirez et al., 2022). The importance of this line of research is, I believe, becoming more salient as the literature appears to be divided on whether these types of exercises are helpful or harmful in terms of LBP (Steele, Bruce-Low, & Smith, 2015; Aasa et al., 2015; Fischer, Calley, & Hollman, 2021; Paryavi et al., 2010; Ramirez et al., 2022).
Initially I would like to conduct/supervise research to establish that therapeutic exercises drawn from Tai Chi and Qigong designed to reduce tension in the erector spinae performed as intended. Dependent outcome measures such as electromyography, as a measure of muscular activation, and infrared spectroscopy, as a measure of muscle compartment blood flow, could be used (Ekström et al., 2020). A progression of this research would be a comparison of these types of exercises in terms of pain reduction and functional improvement with lumbar stabilizing exercises in clinical trials.
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Appendix one:
(This is my contribution to an undergraduate assignment submitted in 2003 as referred to in page 5)
The segmental lumbar stabilisation system as it relates to treatment of low back pain
Introduction
The life time incidence for low back pain is high. Koes et al. (1991) reported that about 80% of the population will suffer back pain in their lives. As if this statistic were not serious enough, Hides, Richardson, & Jull. (1996) reported that while 90% of acute low back pain resolves in two to four weeks, 60 to 80% of people experiencing back pain for the first time will suffer a recurrence within a year.
Treatment approaches are many and varied and include exercise therapy, which is likewise characterized by diversity (Richardson, Jull, & Hides, 2000). Typically, developments in exercise therapy parallel developments in the perceived cause of low back pain (D’Orazio, 1993). Recently, Panjabi (1992) proposed that an unstable spinal joint, i.e., one displaying a large ‘neutral zone’ (defined as the degree of laxity around the joint’s neutral position) was more likely to suffer injury than a stable spinal joint. Modelling studies suggested that the action of muscles spanning individual spinal segments can reduce the neutral zone and thereby increase stability (Panjabi et al., 1989). The muscles involved were defined as ‘local’ muscles by Bergmark (1989) to differentiate them from ‘global’ muscles, which spanned several spinal segments and contributed primarily to gross movement, rather than stability.
Initial stabilization exercise programs emphasized the maintenance of a ‘neutral spine’ under challenge and utilized both global and local muscles (Robinson, 1992). Later, researchers from the University of Queensland developed an approach to stability emphasizing a very specific low load co-contraction of two principal local lumbar muscles, the transversus abdominis and lumbar multifidus (Richardson, Jull, & Hides, 2000). Their exercise approach and the theoretical model from which it developed constitute ‘the segmental lumbar stabilization system’. The following review will document the evidence in support of their system and address such questions as:
- How did the segmental lumbar stabilization system evolve and how does it differ from other spinal stabilization exercise systems?
- What evidence suggests a deep lumbar muscle contribution to local segmental lumbar stability?
- Do muscles such as the respiratory diaphragm contribute to local segmental lumbar stability?
- What devices are used to quantify the efficacy of the exercises and how can they be used clinically to enhance therapeutic efficacy?
Where appropriate, the review will consider possible avenues of future research.
The Local Lumbar Segmental Stabilization System: From Historical Development to Methodological Considerations for Future Research
This section will discuss the development of the local lumbar segmental stabilization system with particular reference to: (1) How it evolved from pre- and co-existing exercise based rehabilitative spinal stabilization programs, (2) The seminal experimental evidence supporting its clinical efficacy, and (3) A discussion of concepts of control methodology as it relates to future research.
Prior to the development of the local lumbar segmental stabilization system, Richardson, Toppenberg, & Jull (1990) were evaluating pre-existing (Robinson 1992) lumbar stabilization systems using surface electromyography to compare exercises that primarily involved trunk flexion (e.g., curl-ups) with those that involved isometric rotational exercise (e.g., bridging with pelvic rotation). Those exercises which selectively activated the external obliques and low lumbar extensors were scored favourably in terms of their spinal stabilizing potential, while those that selectively activated the rectus abdominis were scored unfavourably. The rationale for this scoring system was based on:
The hypothesis…that exercises which involved co-contraction of specific flexors and extensors of the spine without contraction of muscles such as the rectus abdominis were better suited to stabilisation training (Richardson and Jull 1995, pp. 6-7).
However, in 1990 ‘spinal stabilization’ and the muscles that contributed to it were still developing concepts. Therefore, at the time it could reasonably be argued that there was ‘…no published research on…lumbar stabilization [and] its underlying premise of stabilizing motion segments is questionable’ (D’Orazio 1993, p. 40). Equally it could be argued (as it still could be today) that ‘achieving stability is not just a matter of activating a few targeted muscles be they multifidus or any other’ and that ‘…virtually all muscles [rectus abdominis included] work together to create the “balance” in stiffness needed to ensure sufficient stability…’ (McGill et al. 2003, pp. 357-358). This raises the question of what evidence has accrued since 1990 in support of the use of exercises designed with enhancement of the local lumbar segmental stabilization in mind?
First Richardson, Toppenberg, & Comerford (1992) developed a pressure sensor, which could be placed under the lumbar spine in supine lying and measured changes in lumbar curvature during challenges such as single leg raising. The device was later placed under the abdomen in prone lying to assess patients’ ability to draw their abdomen in towards their spine, a manoeuvre designed to specifically co-contract the transversus abdominis and lumbar multifidus. Significantly, it was observed that 90% of low back pain sufferers had difficulty producing and maintaining this manoeuvre. While only 18% of normal individuals found the procedure difficult (Hodges, Richardson, & Jull 1996). This finding was described as a ‘breakthrough in [the] understanding of the muscle dysfunction associated with back pain’ (Richardson and Jull 1995, p. 8) and heralded a change in clinical practice and research from stabilization exercises emphasizing the maintenance of a neutral spine under challenge to exercises emphasizing low load segmental stabilizer co-contraction with an abdominal drawing in manoeuvre.
Up to this point, while the University of Queensland group had made reference to the supposed importance of the transversus abdominis and lumbar multifidus in spinal stabilization, they had not measured the activity (or any other parameter) of these muscles directly. Presumably the invasiveness or technical challenge of such procedures ruled them out at the time. However, this changed in 1994 with the publication of a study using real-time ultrasound imaging to measure the cross-sectional area of the lumbar multifidus in low back pain patients (Hides et al. 1994). The study found that compared to controls, the multifidus was markedly wasted in low back pain sufferers ipsilateral to the painful spinal segment. Two years later Hides, Richardson, & Jull (1996) observed that wasting of this type recovered with exercise therapy designed to co-contract the deep segmental lumbar stabilizers. The study also reported that multifidus wasting was not reversed with spontaneous pain remission in non-exercising controls (Hides, Richardson, & Jull 1996). A follow up study with the same participant cohort found that the experimental group reported markedly lower recurrence of low back pain compared to the control group (Hides, Jull, & Richardson 2001). With regard to the transversus abdominis, Hodges and Richardson (1996) used fine wire electromyography to measure the reaction time of the transversus abdominis in response to perturbation of the trunk. The study found that transversus abdominis reaction time was markedly delayed in low back pain sufferers. To date no study has evaluated the effect of segmental lumbar co-contraction exercises on the reaction time of the transversus abdominis. Taken together these studies indicate that dysfunction of the lumbar multifidus and transversus abdominis is associated with low back pain and that exercises designed to facilitate their co-contraction are able to reverse this dysfunction in the lumbar multifidus and markedly reduce low back pain recurrence.
Methodological considerations and future research
As impressive as the study by Hides, Richardson, & Jull (1996) (and its follow up, Hides, Jull, & Richardson 2001) was in terms of back pain incidence reduction and lumbar multifidus recovery with segmental lumbar co-contraction exercises, it can be criticized methodologically for using a ‘no-treatment’ control. Receiving only advice on bed-rest, pharmaceuticals, and absence from work the control group would have been unlikely to expect the same level of improvement as the experimental group who received twice weekly one-on-one instruction on a promising new therapy. For a recent review on the effect of ‘healing rituals and the placebo effect’ the reader is directed to Kaptchuk (2002). Thus, the difference in expectations between the two groups could have biased the study’s outcome.
To some extent this issue was addressed by O’Sullivan, Twomey, & Allison (1997) in a trial designed to assess the efficacy of segmental lumbar stabilization exercises on chronic back pain patients diagnosed with spondylolysis or spondylolisthesis. The control group (N = 21) in this study undertook exercise of some description (e.g., walking, swimming, or gym) under the advice of their general practitioner. Eight patients attended regular supervised exercise programs (details not published). Therefore, we can assume that thirteen patients received no supervised program. Hence, the control and experimental groups were not comparable in terms of supervised exercise or personal interaction and might, therefore, not be comparable in terms of their expectation of improvement. This may have biased the study’s outcome (reported as long-term pain relief in the treatment group). An alternative, more methodologically rigorous, approach would be to compare the segmental lumbar stabilization exercises with another comparable therapy administered by therapists trained it its use and confident of its value.
McGill (2001) presented an approach to low back stability based on ‘…stabilization exercises that impose the lowest load on the damaged spine’ (McGill et al. 2003, p. 356). According to his research the exercise which produces the greatest stabilization for the least compression is a four point kneeling position with one leg extended at the hip. This exercise was included as an ‘extensor’ exercise in a beginners stabilization program. The recommended ‘anterior abdominal’ exercise in the same program is curl-ups with one leg straight, the other bent to help preserve neutral spine (McGill 2001). It is worth noting that electromyographic studies (McGill et al. 2003) confirm that both of these exercises require marked rectus abdominis, iliocostalis lumborum, and longissimus thoracis activation, each of which are global muscles that the research group at The University of Queensland specifically avoids activating in the early stages of a rehabilitation program when full attention is directed toward improving deep lumbar motor skill. To the best of the author’s knowledge, the exercise program of McGill (2001), as logical as it seems in terms of avoiding spinal compression while maximizing stabilizing potential, has not yet been tested in a clinical trial. Perhaps now is a good time to begin trials designed to assess its worth in comparison to both natural progression (no-treatment control) and to abdominal drawing in exercises as prescribed by the University of Queensland group.
This section has described how the observation that low back pain sufferers could not perform an abdominal drawing in manoeuvre changed the focus from pre-existing exercises emphasizing the maintenance of a neutral spine under challenge to low-load co-contraction of the segmental stabilizing musculature. Comparative control versus no-treatment control was also discussed as it related to proposed future research. The sections that follow will discuss in more detail the muscles involved in segmental lumbar stabilization and the devices used to quantify their function.
(Please note that the sections referred to in the previous sentence were written by my student colleagues in 2003 and have not been included)
References:
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